Current research has underscored the multifactorial nature of TMJ dysfunction, which is now considered as a musculoskeletal disorder involving tissue injury. The immediate cause of the injury is the production of excessive forces either of a macro- or micronature, which are generated through some type of injury-producing oral activity (parafunction). The lesions resulting from this dysfunction are usually expressed subtly through inflammatory, proliferative, and degenerative tissue changes. Furthermore the effects of the dysfunction may be presumed to form at the site where the greatest forces are exerted and host resistance is least, and often the effects of the dysfunction outline the precipitating cause. The misuse of a joint may predispose it to degenerative disease, and it is tempting to consider the possibility that oral motor disorders may cause misuse. The work of Oberg and associates (1971) underscores the deleterious effects of tooth loss on the temporomandibular joints, while other authors (Hansson and Oberg, 1977; Bean and associates, 1977) have demonstrated that articular remodeling results from changes in the mechanical stresses from functional loading imposed on different parts of the joint. Dentists are repeatedly reminded of the vulnerability of oral tissues and their replacements to wear and tear. It is tempting to speculate that wear and tear can also be manifested in the temporomandibular joints, especially as a function of aging and/or the combination of parafunction and depleted dental status. The morphologic appearance of the edentulous state provides very few clues about the wear and tear which may have preceded it. In fact, it tends to mask the tangible biologic price exacted from the temporomandibular joints, and many a dentist has lost sight of joint dysfunction while agonizing over the morphology of the residual ridges. Since so many edentulous patients with temporomandibular joint dysfunction are aged, the clinician finds it impossible to identify the exact etiology in each case, and this may not be possible since the fine demarcation between the major recognized causes of TMJ dysfunction tend to become fuzzy and indistinct with these patients. The overlapping between these groups tends to be the rule rather than the exception. And the overlapping tends to occur not only at the etiological and symptom-description level, but also at the treatment level. The relationship between dental status or occlusion, aging, oral motor disorders and temporomandibular joint changes is still the cause of a great deal of controversy (Zarb and Carlsson, 1979), although indirect evidence suggests that a relationship does exist. Storey (1975) enumerated several principles regarding the physiology of occlusion which he considered to be important. (1) Factors expressing themselves at the occlusal interface (2) (3) Some of these factors are passive in nature. Guidances Other factors are active in nature and involve reflex responses. (4) The determinants of thresholds for occlusal reflex responses (5) All occlusal therapy should be directed at preventing and It is tempting to regard the aging edentulous environment as one with considerable potential for perpetuating reflex responses, since the response depends not only on the magnitude of the extrinsically induced changes (in this case, tooth loss and the insidious but apparently inevitable morphologic changes), but also on the changes induced in the underlying neuromuscular mechanism. Clinical experience and reporting suggest that the vast majority of patients with TMJ dysfunction respond to occlusal therapy. However a small, and to date, undetermined percentage of these patients do not. Their problem may be due to persistence of a parafunctional habit, or to irreversible organic changes, or both. Further research in this area would seem to clarify the combined longitudinal effects of parafunction and tooth loss of the temporomandibular joints. 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